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Venue: Bordeaux School of Neuroscience

The normal aging process is associated with reduced performance on cognitive tasks that require one to quickly process or transform information to make a decision, including measures of speed of processing, executive cognitive function, working and relational memories. Structural and functional alterations in the brain correlate with these age-related cognitive changes, such as loss of synapses, and dysfunction of neuronal networks. It is crucial to develop new approaches that consider the whole neuroanatomical, endocrine, immunological, vascular and cellular changes impacting on cognition.

This 3-week course will cover the fundamentals of cognitive aging -including inter-individual differences, cognitive and brain reserve and risk factors- and highlight the newest functional imaging methods to study human brain function. The Faculty will share the state-of-the-art molecular, optical, computational, electrophysiological, behavioural and epidemiological approaches available for studying the aging brain in diverse model systems. The Students will learn the potential and limitations of these methods, through practical experience in a combination of lectures addressing aging in both humans and animal models and hands-on-projects. They will acquire sufficient practical experience to model, design and interpret experiments and brainstorm on novel technologies and hypotheses to explore the aging of the brain using more integrative and creative approaches.

Keynote speakers:
Hélène Amieva - University of Bordeaux
Adam Antebi - MPI for Biology of Ageing
Carol Barnes - University of Arizona
LucBuée-Centrede Recherche Jean-Pierre Aubert
Gwenaëlle Catheline - University of Bordeaux
Maria Llorens-Martin - Centro de Biologia
Molecular Severo Ochoa
Aline Marighetto - University of Bordeaux
Lars Nyberg - Umeå University
Laure Rondi-Reig - Sorbonne University
Yaakov Stern - Columbia University
Tony Wyss-Coray - Stanford University

Course director: Luísa Lopes
Co-directors: Cheryl Grady and Nora Abrous

Application deadline: 25 May 2020
Stipends are available

Fee : 3.500 € (includes tuition fee, accommodation and meals)

The CAJAL programme offers 4 stipends per course (waived registration fee, not including travel expenses). Please apply through the course online application form. In order to identify candidates in real need of a stipend, any grant applicant is encouraged to first request funds from their lab, institution or government.

Kindly note that if you benefited from a Cajal stipend in the past, you are no longer eligible to receive this kind of funding. However other types of funding (such as partial travel grants from sponsors) might be made available after the participants selection process, depending on the course.

For enquiries, please contact:

General informations
A series of reference-books on the neurobiology of addiction, by Michel Le Moal

With the help of three other international experts, including his long-time accomplice George Koob, Michel Le Moal presents a broad synthesis of what we know about the neurobiology of addiction, in this series of books published by the prestigious Academic Press editions. The first volume addresses in particular the history of addiction theories together with the evolution of the animal models used, to arrive at the more recent discoveries. Each other volume is specifically devoted to a family of drugs of abuse.

The origin of biological lanxit remains unclear, particularly pathological lanxit which nevertheless affects nearly 20% of the population. But thanks lquipe Atip Futures what was up and runs for two years, Anna Beyeler, researcher at Inserm Neurocenter Magendie Bordeaux, sest launches the challenge of some of the mechanisms rvler impliqus in this psychiatric disorder.

The BioProt platform (Biochemistry and Biophysics of Proteins) is the only one under the supervision of the Bordeaux Neurocampus department. Labeled "Research Platform of the University of Bordeaux", it is located in the premises of the Neurocentre Magendie. We met Yann Rufin, a research engineer who has been working on the platform since 2018.

The paper shows that (1) contextual amnesia, produced by the optogenetic inhibition of hippocampal activity (dCA1) during stress, causes PTSD-like hypermnesia in mice, and (2) the re-contextualization of traumatic memory by re-exposure to all trauma-related cues cures PTSD-like memory while promoting normal fear memory.

Al Abed S., Ducourneau E.G., Bouarab C., Sellami A., Marighetto* A., and Desmedt* A.
Preventing and treating PTSD-like memory by trauma contextualization.
Nature Communications.
2020 Aug 24;11(1):4220.
doi: 10.1038/s41467-020-18002-w.

*co-last authorship

(A Study from Desmedt’s team in collaboration with PV Piazza & Lundbeck Lab.)

The paper shows (in collaboration with Lundbeck Laboratory) that acute administration of brexpiprazole, a new antipsychotic drug with pro-cognitive effects in rodents, (0.3 mg/kg) 7 days’ post-trauma persistently prevents the expression of PTSD-like memory in mice, while promoting normal fear memory. Specifically, It specifically blocks the emotional hypermnesia of PTSD while enhancing (with superior efficacy when compared to diazepam, prazosin and escitalopram) memory for the traumatic context, which is impaired in PTSD. Moreover, this treatment also normalizes most of the alterations in the hippocampal-amygdalar network activation associated with PTSD-like memory. These preclinical data indicate that brexpiprazole could represent a new pharmacological treatment of PTSD promoting the normalization of traumatic memory.

Ducourneau E.G., Guette C., Perrot D., Mondesir M., Mombereau C., Arnt J. Desmedt* A. and Piazza* P.V. Brexpiprazole blocks Posttraumatic stress disorder-like memory while promoting normal fear memory. Molecular Psychiatry. 2020 Aug 19.
*co-last authorship.

doi: 10.1038/s41380-020-0852-z
First author

Eva Ducourneau
Team Marighetto/Desmedt
(“Pathophysiology of declarative memory”)

Aline Desmedt
Team Marighetto/Desmedt
(“Pathophysiology of declarative memory”)

Exercise craving potentiates excitatory inputs to ventral tegmental area dopaminergic neurons
Maria‐Carmen Medrano, Imane Hurel, Emma Mesguich, Bastien Redon, Christopher Stevens, François Georges, Miriam Melis, Giovanni Marsicano, Francis Chaouloff
Addiction Biology. 2020-10-05; :

Physical exercise, which can be addictogenic on its own, is considered a therapeutic alternative for drug craving. Exercise might thus share with drugs the ability to strengthen excitatory synapses onto ventral tegmental area (VTA) dopaminergic neurones, as assessed by the ratio of AMPA receptor (AMPAR)-mediated excitatory postsynaptic currents (EPSCs) to NMDA receptor (NMDAR)-mediated EPSCs. As did acute cocaine, amphetamine, or Δ9 -tetrahydrocannabinol (THC) pretreatments, an acute 1-h wheel-running session increased the AMPAR/NMDAR ratio in VTA dopaminergic neurones. To dissect the respective influences of wheel-running seeking and performance, mice went through an operant protocol wherein wheel-running was conditioned by nose poking under fixed ratio schedules of reinforcement. Conditioned wheel-running increased the AMPAR/NMDAR ratio to a higher extent than free wheel-running, doing so although running performance was lower in the former paradigm than in the latter. Thus, the cue-reward association, rather than reward consumption, played a major role in this increase. The AMPAR/NMDAR ratio returned to baseline levels in mice that had extinguished the cued-running motivated task, but it increased after a cue-induced reinstatement session. The amplitude of this increase correlated with the intensity of exercise craving, as assessed by individual nose poke scores. Finally, cue-induced reinstatement of running seeking proved insensitive to acute cocaine or THC pretreatments. Our study reveals for the first time that the drive for exercise bears synaptic influences on VTA dopaminergic neurones which are reminiscent of drug actions. Whether these influences play a role in the therapeutic effects of exercise in human drug craving remains to be established.

Luigi Bellocchio (Marsicano team) and al. in eLife

Cannabis is the most common illicit drug of abuse in the US and globally. In addition, many states in the US, as well as several countries in the world, have legalized the medical and/or recreational use of cannabis. In this rapidly expanding landscape of cannabis use, huge efforts are made to find innovative interventions reducing potential cannabis-evoked harms. Here, we investigated the possible relation between cannabinoids and autophagy, the process of programmed cell “self-digestion”, and asked whether it could be related to the control of motor coordination behavior, one of the best established neurobiological processes impacted by cannabinoids.

We showed that Δ9-tetrahydrocannabinol, the major psychoactive ingredient of cannabis, impairs autophagy and accumulates P62 protein in neurons of the striatum, a brain area that plays a key role in the control of motor coordination. Second, we demonstrate that boosting autophagy, either by pharmacological manipulation (with the FDA-approved mammalian target of rapamycin inhibitor temsirolimus) or by dietary intervention (with the natural, non-toxic disaccharide trehalose), rescues the Δ9-tetrahydrocannabinol-induced impairment of striatal autophagy and motor coordination in mice. Furthermore, we provide evidence that cannabinoid CB1 receptors located on neurons of the striatal direct (stratonigral) pathway, by coupling to mammalian target of rapamycin activation and autophagy inhibition, are indispensable for the motor dyscoordinating activity of Δ9-tetrahydrocannabinol in mice.

Last but not least, using viral mediated genetic manipulation of striatonigral neurons we confirmed that disrupting mammalian target of rapamycin pathway, as well as boosting P62 accumulation in these cells, completely prevents Δ9-tetrahydrocannabinol-induced impairment of striatal autophagy and motor dyscoordination in mice.

Taken together, these findings identify impairment of autophagy as an unprecedented mechanistic link between cannabinoids and motor dyscoordination, and suggest that activators of autophagy might be considered as promising therapeutic tools to treat certain cannabinoid-evoked behavioral alterations.


Inhibition of striatonigral autophagy as a link between cannabinoid intoxication and impairment of motor coordination. Cristina Blázquez, Andrea Ruiz-Calvo, Raquel Bajo-Grañeras, Jérôme M Baufreton, Eva Resel, Marjorie Varilh, Antonio C Pagano Zottola, Yamuna Mariani, Astrid Cannich, José A Rodríguez-Navarro, Giovanni Marsicano, Ismael Galve-Roperh, Luigi Bellocchio, Manuel Guzmán ; eLife 2020;9:e56811 doi: 10.7554/eLife.56811

Andreas Frick (Neurocentre Magendie) has received a Research Award from the Simons Foundation Autism Research Initiative (SFARI).

His project:
Atypical sensory experience is a core feature of Autism Spectrum Disorder (ASD) and may be strongly determinant of other core symptoms of the disorder. Atypical sensory information processing, and associated behavioral symptoms related to the perception of touch, are very common in ASD and exert a strong negative influence on day-to-day life. Nonetheless, there is a surprising paucity of neurobiological studies addressing this aspect of ASD pathology, or specifically attempting to target this symptom for therapeutic rescue. In collaboration with Prof. S. Heinemann (Friedrich-Schiller-University Jena), they are exploring a novel therapeutic strategy for treating sensory symptoms in ASD.